In less than one third of patients undergoing RYGB, steatosis and fibrosis remain unchanged after the intervention [147,148]; however, even if there are no modifications in the histological assessment, a marked decrease in the hepatic expression of different mediators involved in the regulation of fibrogenesis (collagen-alpha 1 (CO1A1), transforming growth factor-1 beta (TGF-1 beta), alpha-smooth muscle actin (α-SMA) and tissue inhibitor of metalloproteinase 1 (TIMP-1)), and inflammation (macrophage chemoattractant protein 1 (MCP-1) and interleukin 8 (IL-8)) has been reported [149]. The gene discussed is CXCL8; the disease is fibrosis.